Prolonged lipopolysaccharide-induced illness elevates glucagon-like peptide-1 and suppresses peptide YY: A human-randomized cross-over trial

Katrine Brodersen*, Maike Mose, Ulla Ramer Mikkelsen, Jens Otto Lunde Jørgensen, Michael Festersen Nielsen, Niels Møller, Anne-Marie Wegeberg, Christina Brock, Bolette Hartmann, Jens Juul Holst, Nikolaj Rittig

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Abstract

Severe systemic inflammation is associated with nausea, loss of appetite, and delayed gastric emptying, which increases hospitalization admission length and mortality rate. There is a lack of human controlled studies exploring gastric emptying rates and underlying mechanisms during inflammatory conditions. We aimed to investigate if systemic inflammation in young men delays gastro-intestinal transit times, lowers motility, and affects gastrointestinal hormone secretion. This substudy of a randomized crossover trial investigated eight healthy young men on two separate occasions; (I) following an overnight fast (healthy conditions/HC) and (II) fasting and bedrest combined with two lipopolysaccharide (LPS) injections of 1 ng kg-1 following an overnight fast and 0.5 ng kg-1 following another 24 h (systemic inflammation/SI). A standardized protein beverage and a SmartPill capsule (a wireless gastrointestinal monitoring system) were swallowed during each occasion. Whole gut transit time was comparable between HC and SI. SI decreased gastric mean pressure peak amplitude (p = 0.04) and increased pH rise across the pylorus and small bowel pH (p = 0.02) compared with HC. Glucagon-like peptide-1 was elevated during SI compared with HC (p = 0.04). Peptide YY was lower during SI compared with HC (p = 0.007). Prolonged LPS exposure combined with fasting and bedrest elevated glucagon-like peptide 1 concentrations, which may play a role for the nausea and loss of appetite typically associated with SI.

OriginalsprogEngelsk
Artikelnummere15462
TidsskriftPhysiological Reports
Vol/bind10
Udgave nummer18
ISSN2051-817X
DOI
StatusUdgivet - sep. 2022

Bibliografisk note

© 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.

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